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phase 2a medicine > introduction to clinical sciences > Flashcards

introduction to clinical sciences Flashcards

1
Q

Define inflammation

A

The body’s response to injury or infection using different types of cells

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2
Q

How can inflammation be sub divided?

A

Acute/ neutrophil mediated or chronic/macrophage/ lymphocyte mediated

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3
Q

what type of cell are neutrophil polymorphs?

A

WBC

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4
Q

where are neutrophil polymorphs made?

A

Bone marrow

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5
Q

what is the lifespan of neutrophil polymorphs?

A

2-3 days

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6
Q

what gives neutrophil polymorphs their name?

A

their multi lobar nucleus

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7
Q

which organelle allows neutrophil polymorphs to carry out their functions?

A

lysosomes allow them to phagocytose bacteria

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8
Q

which cells are the first to arrive at the site of infections?

A

neutrophil polymorphs

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9
Q

where do neutrophil polymorphs die?

A

at the site of infection

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10
Q

what type of cell is a macrophage?

A

WBC

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11
Q

How long do macrophages live for ?

A

months to years

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12
Q

what are the functions of macrophages?

A

phagocytose bacteria, transport material to lymph nodes, presenting it to lymphocytes and triggering a secondary immune response

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13
Q

How long do lymphocytes live for ?

A

years

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14
Q

what do lymphocytes produce?

A

inflammatory mediators and antibodies

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15
Q

which cells provide immunological memory?

A

lymphocytes

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16
Q

Which cells produce collagenous connective tissue?

A

fibroblasts

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17
Q

Describe the sequence of acute inflammation

A
  1. Injury or infection
  2. neutrophils arrive and phagocytose and release enzymes
  3. macrophages arrive and phagocytose
    4.either resolution or progression to chronic inflammation
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18
Q

Give 3 examples of acute inflammation

A
  1. acute appendicitis
  2. frostbite
  3. streptococcal sore throat
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19
Q

describe the sequence of chronic inflammation

A
  1. either progresses from acute inflammation or begins as chronic inflammation
  2. no or very few neutrophils
  3. macrophages, lymphocytes and fibroblasts
  4. can resolve if theirs no tissue damage but often ends up as repair and formation of scar tissue
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20
Q

Give an example of an illness that begins as chronic inflammation

A

infectious mononucleosis

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21
Q

What is a granuloma

A

type of inflammation where collections of macrophages/ histocytes are surrounded by lymphocytes

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22
Q

when may granulomas be significant?

A

when they may be due to a myobacterial infection such as TB or leprosy

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23
Q

what other disease may granulomas be seen in ?

A

Crohn’s disease

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24
Q

when does acute inflammation occur

A

to initial tissue injury

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25
Q

Describe the onset and duration of acute inflammation

A

early onset, short duration

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26
Q

Which cells are involved in acute inflammation

A

monocytes and neutrophils

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27
Q

In 3 steps describe acute inflammation

A
  1. Vascular component, dilation of vessel and increased permeability
    2.exudative component, leakage of protein rich fluid
  2. neutrophil polymorph, recruited to tissue (cellular exudate)
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28
Q

Describe the 4 steps of neutrophil polymorph recruitment

A
  1. migration- increased plasma viscosity and slowing of flow causes neutrophils to migrate to plasmatic zone
  2. adhesion- neutrophil pavementing to endothelium in venules
    3.emigration- neutrophils pass through endothelial cells, basal lamina and vessel wall
    4 diapedesis- RBC’s may also escape from vessel, which is passive transport
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29
Q

Give 6 causes of acute inflammation

A
  1. microbial infections- bacteria and parasites
  2. hypersensitivity reactions - parasites
  3. physical agents- trauma, heat or cold
  4. chemicals - corrosives and acid
    5.bacterial toxins
  5. tissue necrosis- ischaemic infarction
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30
Q

How may acute infection appear?

A
  1. rubor, due to dilation of vessels
    2.calor, heat peripherally
    3,tumor, swelling due to oedema or mass
  2. dolor - pain
    loss of function
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31
Q

Describe the macroscopic appearance of chronic inflammation

A
  1. chronic ulcer
  2. chronic abscess
    3.granulomatous inflammation
  3. fibrosis
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32
Q

Describe the microscopic appearance of chronic inflammation

A

lymphocytes, plasma cells and macrophages, continuing destruction of tissue, no exudation

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33
Q

what can the presence of granulomas and eosinophils suggest?

A

parasite

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34
Q

what are 3 causes of primary chronic inflammation?

A
  1. resistance of infective agent,
    2, endogenous/ exogenous materials
  2. autoimmune disease
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35
Q

Name a cell derived inflammatory mediator

A

histamine

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36
Q

How does repair happen after inflammation?

A

fibroblasts are stimulated by cytokines to proliferate and increase collagen synthesis

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37
Q

what do granulocytes release?

A

prostoglandins

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38
Q

what do prostoglandins cause ?

A

fever and pain

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39
Q

describe 1st intention healing

A

bringing skin together via surgery, fribrin and then collagen join edges

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40
Q

describe 2nd intention healing

A

New cells filling in gap

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41
Q

Describe repair

A

tissues that cant regenerate are replaces by fibrous tissue

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42
Q

name 6 cells that can regenerate

A

hepatocytes, pneumocytes, all blood cells, gut epithelium, skin epithelium, osteocytes

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43
Q

Name 2 cells that cant regenerate

A

myocardial cells, neurones

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44
Q

which model demonstrates the causes of thrombosis?

A

Virchow’s triad, 2 of these are required for thrombosis to happen

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45
Q

Define thrombosis

A

solidification of blood contents that forms within the intact vascular system during life

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46
Q

What are the 3 elements of virchow’s triad

A

1.hypercoagulability
2.stasis of blood
3.vessel wall injury

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47
Q

How is normal blood flow described?

A

laminar

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48
Q

how is interrupted blood flow described

A

turbulent

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49
Q

How does damage to the endothelium trigger thrombus formation?

A

collagen is revealed, this attracts platelets, platelet aggregation begins thrombus formation, fibrin is deposited

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50
Q

How can slow blood flow lead to thrombus formation?

A

causes endothelium nitrous oxide production to reduce, which can lead to deep vein thrombosis

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51
Q

which drug inhibits platelet aggregation?

A

aspirin

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52
Q

How may arterial thrombi appear?

A

cold, painful, pulseless, pale, possible gangrene

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53
Q

what commonly causes arterial thrombi?

A

atheroma

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54
Q

what can arterial thrombi result in?

A

Myocardial infarction, stroke or gnagrene

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55
Q

How may venous thrombi appear?

A

tender, red, swollen

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56
Q

what commonly causes venous thrombi?

A

stasis across valves

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57
Q

what can venous thrombi lead to?

A

deep vein thrombosis or pulmonary embolisms

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58
Q

what are the 4 fates of thrombi?

A
  1. resolved
  2. organised (scar formation)
    3.recanalisation( capillaries grow)
  3. embolus
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59
Q

define emboli

A

mass of material in vascular system able to lodge in a vessel and block its lumen

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60
Q

where do arterial emboli lodge

A

heart, brain or peripheries

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61
Q

where do venous emboli lodge?

A

pulmonary arteries

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62
Q

what determines the impact of a venous embolus?

A

it’s size

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63
Q

Define ischaemia

A

reduction in blood flow to a tissue caused by constriction or blockage of the vessels supplying it

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64
Q

define infarction

A

death of the tissue due to severe or prolonged ischaemia

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65
Q

which organs have a dual supply?

A

Liver, brain, lungs

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66
Q

what impact does dual supply have on infarction?

A

it makes organs less susceptible to infarction

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67
Q

how are non dual supply organs described?

A

end artery supplied

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68
Q

define reperfusion injury

A

damage to tissue during reoxygenation

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69
Q

Describe the steps in atherogenesis

A
  1. Damage to endothelial cells
  2. endothelium secretes chemoattractants
  3. leukocytes migrate and accumulate in intima
    4.foam cells/ macrophages/ T-lymphocytes form fatty streaks
    5.foam cells rupture, releasing lipids
  4. smooth muscle cells migrate from media to intima
  5. dense fibrous cap with necrotic core is formed
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70
Q

How can atheroma lead to ischaemia?

A

partially occluding the lumen of a vessel

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71
Q

How can an atheroma lead to an infarction?

A

The plaque can rupture, forming a thrombus, fully occluding the lumen

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72
Q

Which arteries does atherogenesis affect the most?

A

LAD, circumflex and RCA

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73
Q

What are the risk factors for atherogenesis?

A
  1. Age
  2. smoking
  3. obesity, high serum cholesterol
    4.poorly controlled diabetes
    5.hypertension
    6.family history
  4. being male
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74
Q

what causes cardiac myocyte damage?

A

insufficient oxygen rich blood, increased myocardial workload, coronary artery occlusion, atheroma, valvular disease, anaemia

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75
Q

In ascending order of severity describe cardiac monocyte damage problems

A

stable angina, unstable angina, NSTEMI and STEMI

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76
Q

where do atheromas form

A

high pressure arteries, usually not pulmonary

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77
Q

define apoptosis

A

genetically programmed removal of small groups/ individual cells without release of harmful products to surrounding cells

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78
Q

what is apoptosis important for ?

A

normal physiology

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79
Q

what DNA damage may result in apoptosis of a cells?

A
  1. single strand break
  2. double strand break
    3.cross linkage
  3. base alteration
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80
Q

How does a cell apoptose?

A

it’s an activated caspase enzyme cascade

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81
Q

which protein triggers apoptosis?

A

p53, it can detect enzyme damage

82
Q

Define necrosis

A

unprogrammed cell death due to an adverse event

83
Q

what follows necrosis?

A

acute inflammation

84
Q

what are the different types of necrosis?

A

coagulative, liquefactive, caseous, gangrenous, fat, fibrinoid

85
Q

How does necrosis damage cells

A

mitochondria releases ROS

86
Q

when may you see caseous necrosis?

A

In TB, it has a soft cheese texture

87
Q

Define congenital disease

A

present at birth, not always inherited but usually environmental

88
Q

define inherited disease

A

caused by an inherited genetic abnormality

89
Q

describe acquired disease

A

caused by non genetic factors

90
Q

which cells do autosomal inheritance affect

A

somatic cells rather than sex cells

91
Q

define polygenic inheritance

A

where many genes contribute to disease

92
Q

when do genetic diseases manifest?

A

they may present later in life

93
Q

define hypertrophy

A

increase size of tissue caused by an increase in size of constituent cells

94
Q

define hyperplasia

A

increase in size of tissue due to an increase in the number of constituent cells

95
Q

define atrophy

A

decrease in size of tissue due to a decrease in number of cells or their size

96
Q

define metaplasia

A

change in differentiation from a fully differentiated cell to another fully differentiated cell

97
Q

define dysplasia

A

morphological changes seen in cells in their progression towards being cancer

98
Q

when may you see hypertrophy and hyperplasia in a tissue?

A

in the uterus during pregnancy

99
Q

when may you see atrophy

A

dementia

100
Q

what is the heyflick limit?

A

The number of times a cell can divide

101
Q

what determines the heyflick limit

A

the telomeres shorten with each division, they eventually get so short that they can’t divide

102
Q

what causes dermal elastosis?

A

UV B light causes cross linking of collagen, which causes clumping

103
Q

what causes osteoporosis?

A

increased bone resorption, decreased bon formation and lack of oestrogen

104
Q

what causes cataracts

A

UV B light cross linking proteins in the lense

105
Q

what causes senile dementia?

A

plaques and neurofibrillary tangles

106
Q

what causes sarcopenia?

A

decreased growth hormone, decreased testosterone, increased catabolic cytokines

107
Q

what causes deafness?

A

loss of hair in cochlear, hair cells cant divide and they’re damaged by noise

108
Q

what is the only definitive method for reducing aging ?

A

calorie deficit, metabolites damage cells so reducing the metabolites reduces damage

109
Q

where do basal cell carcinomas invade and how can we treat them?

A

They only invade locally, so complete excision is a cure

110
Q

List the systemic symptoms of leukaemia

A
  1. weight loss
  2. fever
    3.frequent infections
111
Q

what is the muscular symptom of leukaemia?

A

weakness

112
Q

what are the bone and joint symptoms of leukaemia?

A

pain or tenderness

113
Q

what are the psychological symptoms of leukaemia?

A

fatigue and weakness

114
Q

How may the spleen or liver look when someone has leukaemia?

A

enlarged

115
Q

how may the lymph nodes appear in someone with leukaemia?

A

swollen

116
Q

what respiratory problem would someone with leukaemia experience?

A

shortness of breath

117
Q

what symptoms of leukaemia appear on the skin

A
  1. night sweats
  2. easy bleeding and bruising
    3.purplish patches or spots
118
Q

where do carcinomas spread

A

to the lymph nodes that drain the site of carcinoma

119
Q

which carcinomas are commonly spread to the bone?

A

breast, prostate, lung, kidney, thyroid

120
Q

Describe the breast cancer treatment plan

A

confirm the patient has breast cancer
1. has it spread to the axilla?
yes- axillary node clearance
no- has it spread to the rest of the body?
yes- chemo
no- surgery with or without axillary lymph node clearance

121
Q

what may be present after a tumour is completely exercised?

A

micro metastases

122
Q

define adjuvant therapy

A

extra treatment given after surgical excision, ie radiotherapy after a lumpectomy or anti- oestrogen if breast cancer is oestrogen receptor positive

123
Q

define carcinogenesis

A

the transformation of normal cells into neoplastic cells through permanent genetic alterations or mutations

124
Q

what does carcinogenesis apply to ?

A

malignant neoplasms

125
Q

what does oncogenesis apply to?

A

malignant and benign tumours

126
Q

define carcinogens

A

agents known or suspected to cause tumour

127
Q

what are the differences between carcinogenic and oncogenic?

A

carcinogenic is cancer causing and oncogenic is tumour causing

128
Q

what percentage of cancer risk is environmental factors?

A

85%

129
Q

name 3 issues with identifying carcinogens

A
  1. latent periods can last decades
  2. complexity of environment
  3. ethical constraints
130
Q

Give an example of epidemiological evidence of carcinogens

A

hepatocellular carcinoma is common in areas with high hepatitis B/C and mycotoxins

131
Q

Give an occupational carcinogenic risk

A

bladder cancer has a high incidence in aniline dye and rubber industries due to beta naphythylamine

132
Q

Give a behavioural carcinogenic risk

A

smoking and lung cancer

133
Q

Give an example of direct evidence of carcinogens

A

radioactive iodine isotopes released into atmosphere by chernrobyl nuclear reactor 1986, in 1990 there was increased incidence of thyroid cancer in ukranian children

134
Q

describe chemical carcinogens

A

some act directly, however most require conversion from pro-carcinogens to ultimate carcinogens, required enzyme may be ubiquitous or confined to certain organs

135
Q

Describe viral carcinogens

A

cause 10-15% of all cancers

136
Q

Give examples of DNA viral carcinogens

A

1.human herpes virus- kaposi sarcoma
2.epstein Barr virus- Burkitt lymphoma( nasopharyngeal carcinoma)
3.hepatitis B- hepatocellular carcinoma
4. human papillomavirus- squamous cell carcinomas of the cervix, penis, anus, head and neck
4. merkell cell polomavirus- merkell cell carcinoma

137
Q

Give examples of RNA viral carcinogens

A
  1. human T-lymphocytic virus- adult T-lymphocyte leukaemia
  2. Hepatitis C virus- hepatocellular carcinoma
138
Q

give an effect of ionising radiation

A

skin cancer in radiographers

139
Q

give an effect of non ionising radiation

A

lung cancer in uranium minors

140
Q

what does UVA/B increase the risk of?

A

Basal cell carcinoma, melanoma or squamous cell carcinoma

141
Q

what is xerdoma pigmentosum?

A

a hereditary condition that is characterised by extreme sun sensibility, high risk of cancer and other medical issues

142
Q

what does an increase in oestrogen cause?

A

An increase in mammary/ endometrial cancer

143
Q

what does an increase in anabolic steroids cause?

A

an increase in hepatocellular carcinoma

144
Q

which mycotoxin causes hepatocellular carcinoma?

A

aflatoxin B

145
Q

Give 2 examples of parasites causing cancer

A
  1. Clonorchis synesis causes cholangiocarcinoma
  2. Schistosoma causes bladder cancer
146
Q

Give examples of 2 miscellaneous carcinogens

A
  1. asbestos
  2. metals
147
Q

Give 2 examples of host factors affecting risk of developing cancer

A
  1. In India and SE Asia there are increased rates of oral cancer due to betal chewing
  2. Skin cancer is lower in darker skinned people
148
Q

Give 2 examples of inherited predisposition to developing cancer

A
  1. familial polyposis coli
    2.retinoblastoma
149
Q

what effect does age have on cancer risk?

A

it increases with age, due to the incidence of genetic mutations being acquired through life

150
Q

How does alcohol usage affect the risk of cancer

A

increases the risk of mouth, oesophagus, liver, colon, breast and kidney cancer

151
Q

How does exercise affect the risk of cancer

A

reduces risk of colon and breast cancer

152
Q

How does unprotected sex affect thee risk of cancer?

A

increased risk of HPV related cancers

153
Q

what is a premalignant lesion?

A

An identifiable local abnormality associated with increased risk of malignancy at that site

154
Q

Give 4 examples of premalignancy lesions

A
  1. colonic polyps
  2. cervical dysplasia
    3.ulcerative colitis
  3. undescended testes
155
Q

Give 1 example of transplacental exposure causing an increased risk of cancer.

A

diethylstilboestrol, causes increased risk of vaginal cancer

156
Q

Define neoplasia

A

A lesion resulting from autonomous or relatively autonomous abnormal growth of cells which persists after the initiating stimulus has been removed

157
Q

describe the 2 spectrums that neoplasia is on

A

1.malignant to benign
2. fatal to subclinical

158
Q

which 2 things make up neoplasia?

A
  1. neoplastic cells and stroma
159
Q

describe neoplastic cells

A

derived from nucleated cells, usually monoclonal, growth pattern related to parent cells, synthetic activity related to parent cells

160
Q

describe stroma

A

connective tissue framework, mechanical support and nutrition

161
Q

what is tumour angiogenesis?

A

when a tumour reaches larger than 2mm in size it has to become vascularised to survive

162
Q

what are the 2 methods of classifying tumours?

A

1.behavioural, benign, borderline or malignant
2.histogenetic, cell of origin

163
Q

Describe benign neoplasms

A

localised, non invasive, slow growth, low mitotic activity, closes resemblance to normal tissue, circumscribed or encapsulated, nuclear morphometry often normal, necrosis is rare, ulceration is rare, grow on mucosal surfaces, often exophytic ( grow up and out)

164
Q

why are benign tumours problematic?

A
  1. they put pressure on adjacent structures
  2. obstruct flow
  3. produce hormones
  4. transformation into malignant neoplasms
  5. anxiety
165
Q

Describe malignant neoplasms

A

invasive, metastases, rapid growth rate, variable resemblance to normal tissue, poorly defined or irregular border

166
Q

Who is the best snack?

A

You.

167
Q

Describe the cellular properties of malignant neoplasms

A

Hyperchromatic nuclei, pleomorphic nuclei, increased mitotic activity, necrosis is common, ulceration is common, grow on skin and mucosal surfaces, often have endophytic growth

168
Q

Why do malignant neoplasms cause problems?

A
  1. destruction of adjacent tissues
  2. metastases
  3. blood loss from ulcers
  4. obstruction of flow
  5. hormone production
  6. paraneoplastic effects
  7. anxiety and pain
169
Q

How are malignant neoplasms circumscribed?

A

Poorly

170
Q

where may neoplasms arise from?

A

epithelial cells, connective tissue, lymphoid, haematopoietic organs

171
Q

What is the suffix for most neoplasms

A

‘-oma’

172
Q

Describe 2 benign epithelial neoplasm prefixes

A

1.papilloma, benign tumour of non glandular non secretory epithelium ie squamous cell papilloma
2. Adenoma, benign tumour of glandular or secretory epithelium, ie colonic adenoma

173
Q

describe the prefix for malignant epithelial neoplasms

A

carcinoma, malignant tumour of epithelial cells ie urothelial carcinoma

174
Q

How do you describe a malignant neoplasm of glandular epithelium

A

adenocarcinoma

175
Q

Give 4 examples of benign connective tissue neoplasms (normal names)

A
  1. Lipoma
  2. Chondroma- cartilage
  3. Osteoma- bone
  4. Angioma- vascular
176
Q

Give 3 examples of benign connective tissue neoplasms (abnormal names)

A
  1. Rhabdomyoma - striated muscle
  2. Leiomyoma, smooth muscle
  3. Neuroma, nerves
177
Q

What are malignant neoplasms of the connective tissue prefixed with?

A

sarcoma

178
Q

when the cell type of origin is unknown what is a tumour called?

A

anaplastic

179
Q

give the exceptions as to which ‘-om’as’ are not neoplasms

A

granulomas, mycetoma, tuberculoma

180
Q

Give 3 examples of malignant neoplasms that aren’t carcinoma or sarcoma

A

1.melanoma, malignant neoplasms of melanocytes
2. mesothelioma, malignant neoplasm of mesothelial cells
3. lymphoma, malignant neoplasm of lymphoid cells

181
Q

Give 4 examples of eponymously named tumours

A
  1. Burkitt’s lymphoma
  2. Ewing’s sarcoma
  3. Grawitz tumour
  4. Kaposi sarcoma
182
Q

which cell do all immune cells develop from?

A

A multipotential hematopoietic stem cell called a hemocytoblast

183
Q

What 2 cell types does a hemocytoblast differentiate into?

A

a common myeloid progenitor or a common lymphoid progenitor

184
Q

Describe the different cells that derive from a common myeloid progenitor

A
  1. megakyocyte
  2. erythrocyte
  3. mast cell
  4. myeloblast
185
Q

which cells doe thrombocytes arise from?

A

megakaryocytes

186
Q

which cells arise from a myeloblast?

A
  1. basophils
  2. neutrophil
  3. eosinophil
  4. monocyte
187
Q

which cell does a macrophage arise from?

A

A monocyte

188
Q

which cells arise from common lymphoid progenitors

A
  1. natural killer cells or small lymphocytes
189
Q

which cells does a small lymphocyte give rise to?

A

T lymphocytes or B lymphocytes

190
Q

which cells do plasma cells arise from?

A

B cells

191
Q

where doe all immune cells originate?

A

Bone marrow

192
Q

where do T cells mature?

A

thymus

193
Q

where do B and T cells accumulate?

A

Lymph nodes

194
Q

where are red blood cells removed?

A

The spleen

195
Q

what can cause splenomegaly (enlarged spleen)?

A

Leukaemias

196
Q

Describe the innate immune system

A

non- specific defence system you were born with, an example is mucus or inflammation

197
Q

describe adaptive immunity

A

acquired defence system to destroy/ prevent growth of pathogens , ie antibodies

198
Q

how fast is the adaptive immune system compared to the innate system?

A

slow, it takes days to weeks whereas the innate is fast, hours to days

199
Q

describe the regulation in the innate and adaptive system

A

positive and negative in innate and just positive in adaptive

200
Q

describe the amplification in the innate and adaptive immune response

A

an insignificant amount in the innate and a lot in the adaptive

phase 2a medicine (3 decks)

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